Prophage induction by 4 antimalaria drugs (daraprim, fansidar, nivaquine and camoquine) and in combination with aflatoxin B1

• Published in: Mutation Research/Genetic Toxicology Vol. 222; no. 4; pp. 311 - 316
• Main Authors: Fasunon, O D, Uwaifo, A O
• Format: Journal Article
• Language: English
• Published: Netherlands 01.04.1989
• Subjects: Aflatoxin B1; Aflatoxins - toxicity; Amodiaquine - toxicity; Antimalarials - toxicity; Chloroquine - toxicity; Dose-Response Relationship, Drug; Drug Combinations - toxicity; Drug Synergism; Escherichia coli - drug effects; In Vitro Techniques; Lysogeny - drug effects; Mutagenicity Tests; Pyrimethamine - toxicity; Sulfadoxine - toxicity
• ISSN: 0027-5107; 0165-1218
• DOI: 10.1016/0165-1218(89)90105-5

The abilities of 4 antimalaria drugs (Daraprim, Fansidar, Nivaquine and Camoquine) on their own and in combination with aflatoxin B1 to induce prophage in tester strains E. coli D21 and D22 were studied. The 4 drugs were found to induce prophage in the tester strains; Daraprim and Fansidar without the need for activation by liver mixed function oxidases (S9 microsomal fraction), while Nivaquine and Camoquine did require activation by this system. Aflatoxin B1 was used as a positive control in all the tests. The combined effects of each of the drugs with aflatoxin B1 were lower than that of the individual drugs acting alone. From these results, it may be concluded that the drugs may, on their own, pose a carcinogenic hazard to the population in the Nigerian environment exposed to them. In addition, the depression of prophage induction observed when the drugs were combined with aflatoxin B1 may be indicative of a common target site of action in the tester strains.